Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable chinical interest, severe neurological manifestations may occur days or weekes after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
Animal ; Carbon Monoxide Poisoning/complications/*physiopathology ; Human

Brain Diseases ; etiology ; Carbon Monoxide Poisoning ; complications ; Humans ; Pulmonary Embolism ; complications

Carbon monoxide intoxication has long been one of the most serious public health problems in Korea. This is mainly due to the wide use of anthracite coal briquettes as domestic fuel for cooking and under-the floor heating. One hundred and seven cases of CO intoxicated children hospitalized at Yonsei Medical center from January 1970 to December 1986 have been investigated clinically. The sex ratio was 1.3:1 (male 60 cases, female 47 cases) with the peak incidence occuring in patients between 12 and 14 years of age (28%). The most common symptoms were vomiting convulsions and headache; and the most frequent signs were altered mental state, increased deep tendon reflex and a positive Babinski sign. The outcome of patients was as follows: 4 cases (3.7%) expired, 77 cases (72.0%) recovered without neurologic sequelae and 26 cases (24.3%) survived with neurologic sequelae. The neurologic sequelae included persistent convulsions (7 cases), cortical blindness (3 cases), peripheral neuropathy (2 cases) and delayed neurologic sequelae (11 cases). Neurologic sequelae occurred most frequently in comatose patients (45.5%) and least often in mentally alert patients (6.1%), more frequently m patients exposed to CO gas for more than 8 hours than in those exposed for less than 8 hours, and in patients who did not receive hyperbaric oxyen therapy(29.4%) than in those who did(19.6%). Delayed neurologic sequelae were mental retardation (72.7%), epilepsy (36.4%), mutism (18.2%) etc. The lucid interval in 11 cases of delayed neurologic sequelae ranged from 2 to 20 days. The results of this study suggest that every patient exposed to CO gas should receive prompt and efficient oxygenation including hyperbaric oxygen therapy and that expeditious reduction of cerebral edema maybe of value. The importance of providing follow-up facilities in anticipation of a relapse of the delayed neurologic sequelae has been established.
Adolescent ; Carbon Monoxide Poisoning/complications* ; Carbon Monoxide Poisoning/radiography ; Carbon Monoxide Poisoning/therapy ; Central Nervous System Diseases/chemically induced* ; Child ; Child, Preschool ; Female ; Human ; Hyperbaric Oxygenation ; Male ; Tomography, X-Ray Computed

OBJECTIVETo investigate clinical and imaging characteristics of delayed encephalopathy after carbon monoxide poisoning(DEACMP).

METHODSA retrospective and comparative analysis of neurological manifestations, course, periods of false-cure, prognosis and neuroimaging findings were conducted in 198 patients with DEACMP.

RESULTSOf these patients, 60.1% obtained an initial recovery within 30 d, 23.7% within 31-60 d and 14.6% over 60 d. Total clinical rate was 32.8%, and effectiveness rate 70.1%. According to imaging findings, 15.2% patients were found to have bilateral lesions of basal ganglion, and 70.0% with lesions of subcortical white matter, 12.6% with lesions of two types above mentioned and 2.1% with no lesions. The intervals between onset of illness and initial recovery were (44.6 +/- 10.1), (38.2 +/- 11.9), (61.3 +/- 17.0) d, and (7.5 +/- 2.4) d respectively. Imaging findings can demonstrate the severity of brain injury, but not necessarily parallel to the improvement of illness, for which SPECT proves more useful.

CONCLUSIONSDEACMP is involved in ischemic brain injury and a self-limited illness.

Acute Disease ; Adolescent ; Adult ; Carbon Monoxide Poisoning ; complications ; Cardiomyopathies ; etiology ; Child ; Female ; Humans ; Male ; Middle Aged

A 45-year-old Korean woman visited our hospital complaining of poor vision after carbon monoxide (CO) poisoning. We have confirmed the presence of a point mutation at position 11778 in the ND4 gene of mitochondrial DNA. This case suggests that CO poisoning may precipitate the clinical expression of Leber's hereditary optic neuropathy (LHON). To our knowledge, this would be the first case report of clinical expression of LHON precipitated by CO poisoning.
Carbon Monoxide/adverse effects ; Carbon Monoxide Poisoning/*complications ; DNA Damage ; DNA, Mitochondrial/genetics ; Female ; Humans ; Middle Aged ; Optic Atrophies, Hereditary/*etiology/genetics ; *Point Mutation ; Visual Acuity

Twenty cases of peripheral neuropathy as sequelae of carbon monoxide intoxication have been analyzed clinically. The incidence of pheripheral neuropathy was 0.84% in a total of 2,360 cases and 3.64% in 549 admitted cases of carbon monoxide intoxication. The ratio of male to female was 1:1.2 (9:11). Their ages ranged from 17 to 52 years (mean 29.5 years), with a peak incidence in the 3rd decade (55%). The lower extremity was exclusively involved, and the left side was more involved than the right. Symptoms were a burning sensation, tingling sensation, shooting pain and weakness. Other associated sequelae were local swelling, acute renal failure, delayed neurologic sequelae, and Volkman's contracture in that order. Of 20 cases, 6 showed abnormal findings in the electromyogram only, and 14 were abnormal in both electro-myogram and nerve conduction velocity. Fifteen cases recoved within 3 to 6 months.
Adolescent ; Adult ; Carbon Monoxide Poisoning/complications* ; Extremities ; Female ; Human ; Male ; Middle Age ; Peripheral Nervous System Diseases/etiology*

One month following carbon monoxide poisoning, a 39 year-old man developed incontinence, memory impairment, disorientation and emotional instability. He was hospitalized 7weeks later, and during hospitalization he exhibited myoclonic movements of the neck and lower limbs. He was given piracetam intravenously for 11 days. The myoclonus was significantly reduced by the third day of treatment and had disappeared by the seventh day. There was no recurrence following cessation of treatment.
Adult ; Carbon Monoxide Poisoning/complications* ; Human ; Male ; Myoclonus/drug therapy ; Myoclonus/etiology* ; Piracetam/therapeutic use* ; Pyrrolidinones/therapeutic use*

Adult ; Carbon Monoxide Poisoning ; complications ; psychology ; Humans ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; diagnosis ; physiopathology ; Suicide, Attempted ; psychology

Adult ; Aged ; Aged, 80 and over ; Carbon Monoxide Poisoning ; complications ; Female ; Humans ; Interleukins ; blood ; Male ; Middle Aged ; Neurotoxicity Syndromes ; blood ; etiology